Primary glomerular nephritis (i.e. a glomerular disease in which glomeruli of the kidneys are affected) is clinically classified into seven types; i.e. acute nephritis after infection with hemolytic streptococcus, crescentic glomerulonephritis (rapidly progressive nephritis), IgA nephropathy, membranous nephropathy, membranous proliferative nephritis, focal glomerulosclerosis and minimal change nephrotic syndrome. Generally, the diseases other than acute nephritis after infection with hemolytic streptococcus, crescentic glomerulonephritis and minimal change nephrotic syndrome are collectively called “chronic glomerular nephritis,” and in many cases the cause and time of the onset of chronic glomerular nephritis are not well elucidated. In chronic glomerular nephritis the pathological process is generally progressive, and often results in renal failure or requirement for dialysis.
A drug which radically cures such a glomerular disease has not yet been developed, and thus a steroidal agent, an antiplatelet agent, an anticoagulant, an immunosuppressant or a similar drug has been employed for the purpose of pharmacotherapeutically suppressing or retarding the progression of the disease to the point of requiring dialysis. In recent years, a renin-angiotensin system inhibitor (e.g., an angiotensin II receptor blocker (ARB)) has been employed for such a purpose.
Among the aforementioned drugs, an ARB has been reported to exhibit the effect of suppressing an increase in systemic blood pressure through inhibition of angiotensin II (type 1) receptor. In addition, an ARB has been reported to exhibit, in the kidneys, for example, the effect of reversing the increase in intraglomerular pressure due to dilation of efferent glomerular arterioles, and the effect of suppressing proliferation of mesangial cells. Therefore, use of this drug has been considered to contribute toward suppressing progression or exacerbation of a glomerular disease (see Non-Patent Documents 1 and 2).
In renal diseases, the degree of worsening of hyperlipidemia has been reported to be statistically correlated with the degree of proteinuria or impaired renal function. Therefore, a therapeutic agent for hyperlipidemia (e.g., simvastatin) has been employed in the therapy of a renal disease for the purpose of removing hyperlipldemia, which is a factor exacerbating the disease.
However, when an ARB or a hyperlipidemia therapeutic agent is employed singly, the effect of the drug in the therapy of a renal disease is limited, and is not sufficient.    Non-Patent Document 1: Lassila M, et al. Antiproteinuric Effect of RAS Blockade: New Mechanisms. Curr Hypertens Rep. 6 (5): pp. 383-92, 2004    Non-Patent Document 2: Weiss R H, et al.: TGF-β- and angiotensin-II-induced mesangial matrix protein secretion is mediated by protein kinase C. Nephrol Dial Transplant. 13 (11): pp. 2804-13, 1998